Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:6.3.4.6 (urease)
 7,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebral neurogenic vasodilation is mediated predominantly by nitric oxide (NO). Thus, NO was suggested to be a vasodilator transmitter. In the present study, the possibility that cerebral perivascular nerves can convert citrulline to arginine was examined to ascertain that NO is derived directly from these perivascular nerves. To investigate the uptake of citrulline and its conversion to arginine, both fresh and cold storage-denervated porcine cerebral arteries with or without endothelial cells were incubated at 37 degrees C for 2 hr in Krebs-Ringer bicarbonate buffer containing 0.5 mM purified [14C]ureido-citrulline. The formation of [14C]arginine was measured as 14CO2 by a coupled enzymatic assay involving arginase and urease. The abolishment of nitric oxidergic nerves was verified by NADPH-diaphorase (constitutive NO synthases) histochemical staining method. The results indicated that there was an active conversion of [14C]arginine from [14C]citrulline in nerve-intact arteries denuded of endothelial cells. The conversion was significantly decreased in denervated arteries, accompanied by a significantly reduced citrulline uptake into these denervated arteries. L-Glutamine, but not L-glutamate, gamma-aminobutyric acid, or nitro-L-arginine significantly inhibited the uptake of [14C]citrulline into cerebral perivascular nerves. These data suggest that porcine cerebral vasodilator nerves are nitric oxidergic in nature and citrulline, co-produced with NO by NO synthases from arginine, can be recycled to form arginine in these nerves. The existence of a functional arginine-citrulline cycle may contribute to a constant supply of L-arginine and suggests a neuronal source of NO for inducing cerebral vasodilation.
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PMID:Arginine synthesis from citrulline in perivascular nerves of cerebral artery. 775 95

BACKGROUND: This study was designed to determine whether Helicobacter pylori forms part of the normal microenvironment of the appendix, whether it plays a role in the pathogenesis of acute appendicitis, and whether it is associated with increased expression of inducible nitric oxide synthetase (iNOS) in appendicular macrophages. METHODS: Serology for H. pylori was performed on 51 consecutive patients undergoing emergency appendicectomy. Appendix samples were tested for urease activity, cultured and stained for H. pylori, graded according to the degree of inflammatory infiltrate, and probed immunohistochemically for iNOS expression. RESULTS: The mean age of the patients was 21 (range 7-51) years. Seventeen patients (33 per cent) were seropositive for H. pylori but no evidence of H. pylori was found in any appendix specimen. However, an enhanced inflammatory cell infiltration was observed in seropositive patients (P < 0.04) and the expression of macrophage iNOS in the mucosa of normal and inflamed appendix specimens was increased (P < 0.01). CONCLUSION: H. pylori does not colonize the appendix and is unlikely to be a pathogenic stimulus for appendicitis. Priming effects on mucosal immunology downstream from the foregut may occur after infection with H. pylori.
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PMID:Nitric oxide synthetase and Helicobacter pylori in patients undergoing appendicectomy. 1063 58